Rumplessness of chicken embryos produced by the injection of insulin and other chemicals

Abstract

Incidental to other investigations it was observed that the injection of solutions of certain chemicals into unincubated chicken eggs led to the appearance of increased numbers of rumpless embryos and chicks. It was decided to make a systematic study of this problem, and the following is a first report on our work. MATERIAL AND METHODSThe experiments were done chiefly with eggs from White Leghorn matings, but in one instance eggs from matings of Creeper fowl were used for a series of tests (insulin). Eggs were collected for periods of 1 week. During this time they were kept in an air-conditioned storage room. Eggs from the same mothers were distributed as evenly as possible into experimental and control groups. Prior to injecting the eggs they were allowed to stand in upright position for about 24 hours. After cleaning with alcohol a hole was drilled into the shell with a dental drill. This was done near the level of the short axis of the eggs. A tuberculin syringe was used for the injections, together with a no. 37, &inch hypodermic needle. The amount of fluid iqjected was always 0.05 cc. The hole in the shell was sealed with Scotch tape. Treated and control eggs were incubated in the same forced-draft incubator.The particular length of hypodermic needle used was chosen in order to be certain that the solutions would be injected into the yolk of the eggs. Was this actually accomplished and did the injected material not escape through the needle hole in the yolk membrane7 Information in this respect was obtained by injecting eggs with 0 . 0 5~~. of India ink, letting the eggs stand for 24 hours, hard-boiling them, and then opening them by a cut through their long axis. It was found that in each instance the major part of the ink was within the yolk, although traces were found along the path of the needle.

In human gestational diabetes mellitus congenital malformations are related to pre-pregnancy body mass index and to severity of diabetes

“…A second possible mechanism is hyperinsulinaemia itself. Insulin was recognised as a teratogen in chicken embryo in 1945 [27]. In the absence of specific antibodies [28], insulin is generally considered not to cross the human placenta [29] but studies do not adequately address early pregnancy.…”

Urorectal septum malformation sequence: Insights into pathogenesis

“…Maternal diabetes is associated with developmental field defects (Chen et al, 1998;Padmanabhan et al, 1999), but animal studies show that hyperglycemia is not the only causal factor because insulin therapy failed to abolish teratogenic potential of serum from diabetic rats (Wentzel and Eriksson, 1996). Moreover, insulin may cause rumplessness in chicks (Landauer, 1945). Thus, the association of maternal diabetes with HLXB9 expression in the fetal pancreas, and mutations in the gene in the Currarino triad is intriguing.…”

Embryotoxic effects of brief maternal insulin-hypoglycemia during organogenesis in the rat.

“…To accomplish this, we used insulin infusions by square-wave delivery to effect circumscribed periods ofhypoglycemia in mothers. We simultaneously maintained paired insulin-infused control animals at normoglycemia with exogenous dextrose to test for any potential teratogenic effects of insulin per se (15)(16)(17)(18)(19). We limited the duration of the hypoglycemia to 1 h and opted for a mild glucopenia that would not disrupt maternal consciousness in order to mimic the type ofhypoglycemia that may occur during clinical attempts at strict diabetes control.…”

“…The relevance of those observations to the generally mild and evanescent hypoglycemia that occurs during clinical attempts at strict diabetes control has therefore been unclear. Furthermore, none of these earlier studies evaluated the potential for direct effects ofinsulin on the conceptus, which are of some concern in view of the embryotoxic actions that have been ascribed to insulin in the chick (15)(16)(17)(18)(19). Our experimental design enabled us to overcome these limitations and thereby to demonstrate for the first time that a relatively mild and briefepisode of maternal insulin-induced hypoglycemia during early mammalian organogenesis may be embryotoxic, and that this phenomenon is independent of any direct toxic effects of insulin.…”